| First Author | Puleston DJ | Year | 2014 |
| Journal | Elife | Volume | 3 |
| PubMed ID | 25385531 | Mgi Jnum | J:218211 |
| Mgi Id | MGI:5616987 | Doi | 10.7554/eLife.03706 |
| Citation | Puleston DJ, et al. (2014) Autophagy is a critical regulator of memory CD8(+) T cell formation. Elife 3 |
| abstractText | During infection, CD8(+) T cells initially expand then contract, leaving a small memory pool providing long lasting immunity. While it has been described that CD8(+) T cell memory formation becomes defective in old age, the cellular mechanism is largely unknown. Autophagy is a major cellular lysosomal degradation pathway of bulk material, and levels are known to fall with age. In this study, we describe a novel role for autophagy in CD8(+) T cell memory formation. Mice lacking the autophagy gene Atg7 in T cells failed to establish CD8(+) T cell memory to influenza and MCMV infection. Interestingly, autophagy levels were diminished in CD8(+) T cells from aged mice. We could rejuvenate CD8(+) T cell responses in elderly mice in an autophagy dependent manner using the compound spermidine. This study reveals a cell intrinsic explanation for poor CD8(+) T cell memory in the elderly and potentially offers novel immune modulators to improve aged immunity. |
